PEG-MGF

PEG-MGF is a pegylated form of MGF that extends half-life and stability. It activates muscle stem cells, supports protein synthesis, and offers neuro/cardioprotection. Often combined with IGF-1 LR3 for enhanced myogenesis; may aid cholesterol reduction, immune function, and sarcopenia.

- Enhance muscle growth and recovery

- Support tissue healing and reduce muscle loss

Mechanism of Action

How this peptide works in the body

Muscle Growth and Repair:

PEG-MGF binds to insulin-like growth factor 1 receptors (IGF-1R) on muscle cells, activating the PI3K/Akt/mTOR signaling pathway. This cascade enhances mammalian target of rapamycin (mTOR) activation, driving muscle hypertrophy and hyperplasia by promoting protein synthesis and cellular growth. Additionally, it activates muscle satellite cells, leading to increased muscle mass, repair, and regeneration.

Paracrine and Autocrine Signaling:

PEG-MGF exerts paracrine effects by promoting the local release of fibroblast growth factor (FGF), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF). These factors enhance angiogenesis, extracellular matrix remodeling, and muscle fiber repair. Autocrine signaling triggers IGF-1R-mediated activation of the ERK1/2-MAPK pathway, further supporting cellular growth, survival, and metabolic adaptation in skeletal, cardiac, and neural tissues.

Prolonged Activity Through PEGylation:

PEGylation extends PEG-MGF's half-life by shielding it from enzymatic degradation and renal clearance, ensuring sustained receptor binding and prolonged downstream signaling. This results in continuous mTORC1-mediated protein synthesis, inhibition of the ubiquitin-proteasome system, and suppression of muscle atrophy-related genes such as MuRF-1 and Atrogin-1, preventing protein breakdown and muscle wasting.

Neuroprotection:

PEG-MGF enhances neuronal survival by increasing brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) expression. This activates TrkB receptors, triggering the PI3K/Akt and ERK1/2 pathways, which promote neuronal plasticity, dendritic growth, and synaptic remodeling. Additionally, PEG-MGF inhibits caspase-3-dependent apoptosis, reducing ischemia-induced neuronal loss.

Cardiac Repair:

PEG-MGF modulates IGF-1/Akt signaling in cardiac myocytes, reducing oxidative stress by upregulating superoxide dismutase (SOD) and catalase (CAT). It prevents ischemia-induced myocardial remodeling by inhibiting TGF-β/Smad3 signaling, reducing fibrosis and promoting cardiomyocyte survival. By enhancing VEGF-mediated angiogenesis, it supports vascular repair and improves cardiac function following ischemic injury.